Triamcinolone Acetonide is a synthetic glucocorticoid with anti-inflammatory, antiproliferative, antiangiogenic, and anti-permeability properties[1]. Triamcinolone Acetonide binds to and activates the glucocorticoid receptor, producing anti-inflammatory responses such as down-regulating pro-inflammatory cytokine expression, preventing prostaglandin and leukotriene synthesis and arachidonic acid release, and activating anti-inflammatory transcription factors such as lipocortins[2]. Triamcinolone Acetonide reduces retinal vascular permeability, enhances retinal barrier function, decreases vascular leakage, and alters the localization of tight junction proteins[3]. Triamcinolone Acetonide has been widely used to alleviate ocular inflammation and intraocular edema, and to promote blood vessel contraction[4].
In vitro, Triamcinolone Acetonide inhibited the growth of bone marrow-derived mesenchymal stem cells (MSCs) in a dose- and time-dependent manner, with IC50 values at 24 and 48h of 80nM and 19nM, respectively[5]. Incubation with Triamcinolone Acetonide at a dose of 1mg/ml for 7 days reduced the viability and increased apoptosis of human rotator cuff-derived cells, and caused the cell morphology to change into flattened polygons[6]. Treatment with 400µg/ml Triamcinolone Acetonide for 24 hours induced death of rat primary retinal cells, accompanied by increased intracellular reactive oxygen species (ROS) levels and enhanced phosphorylation levels of p38, JNK, and Erk[7].
In vivo, a single intra-articular injection of Triamcinolone Acetonide (25µg) alleviated synovial inflammation and synovial thickening and reduced type II collagen deposition at the defect site within 28 days in a mouse cartilage defect model[8]. On days 15, 30, and 45 after construction of the mouse scar model, 40mg/ml Triamcinolone acetonide (0.3ml) was injected into the back wounds, respectively, which inhibited scar formation, improved skin tissue status, and reduced the protein and mRNA expression levels of COL1, COL3, and α-SMA in scar tissue[9].
References:[1] Chang Y S, Wu C L, Tseng S H, et al. Cytotoxicity of triamcinolone acetonide on human retinal pigment epithelial cells[J]. Investigative ophthalmology & visual science, 2007, 48(6): 2792-2798.
[2] Paik J, Duggan S T, Keam S J. Triamcinolone Acetonide Extended-Release: A Review in Osteoarthritis Pain of the Knee: J. Paik et al[J]. Drugs, 2019, 79(4): 455-462.
[3] Imai S, Otsuka T, Naito A, et al. Triamcinolone acetonide suppresses inflammation and facilitates vascular barrier function in human retinal microvascular endothelial cells[J]. Current Neurovascular Research, 2017, 14(3): 232-241.
[4] Jonas J B. Intravitreal triamcinolone acetonide for treatment of intraocular oedematous and neovascular diseases[J]. Acta ophthalmologica scandinavica, 2005, 83(6): 645-663.
[5] Kumlin M, Ungerstedt J, Cai H, et al. The functional and molecular impact of triamcinolone acetonide on primary human bone marrow mesenchymal stem cells[J]. Scientific Reports, 2023, 13(1): 21787.
[6] Harada Y, Kokubu T, Mifune Y, et al. Dose-and time-dependent effects of triamcinolone acetonide on human rotator cuff-derived cells[J]. Bone & Joint Research, 2014, 3(12): 328-334.
[7] Chung H, Hwang J J, Koh J Y, et al. Triamcinolone acetonide-mediated oxidative injury in retinal cell culture: comparison with dexamethasone[J]. Investigative ophthalmology & visual science, 2007, 48(12): 5742-5749.
[8] Wesdorp M A, Capar S, Bastiaansen-Jenniskens Y M, et al. Intra-articular administration of triamcinolone acetonide in a murine cartilage defect model reduces inflammation but inhibits endogenous cartilage repair[J]. The American Journal of Sports Medicine, 2022, 50(6): 1668-1678.
[9] Wu Z, Huang D, Xie J, et al. Triamcinolone acetonide suppressed scar formation in mice and human hypertrophic scar fibroblasts in a dose-dependent manner[J]. Cellular and Molecular Biology, 2023, 69(8): 226-231.